Search Results

You are looking at 1 - 3 of 3 items for :

  • "epidermal growth factor receptor" x
  • By Author: Eskandar, Emad x
Clear All
Restricted access

Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010

, AZ), Kenneth Aldape , MD, (Houston, TX), and Arnab Chakravarti , MD, and (Columbus, OH) Griffith R. Harsh IV , MD 8 2010 113 2 A430 A430 This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose. 2010 Introduction: Aberrant activation of the epidermal growth factor receptor (EGFR) oncoprotein is a molecular hallmark of glioblastomas. Two-thirds of tumors with excessive EGFR activation show alteration of the EGFR gene. The

Free access

Epidermal Growth Factor Receptor (EGFR), termed EGFRvIII. Through an RNAi screen, we identified that the Polo-like Kinase 1 (PLK1) mediate cellular adaptation to EGFRvIII induced DNA damage accumulation through its modulation of homologous recombination (HR). Consistent with this role, PLK1 inhibition by BI2536 treatment enhanced the tumoricidal effects of the temozolomide (TMZ) in vitro and in vivo. Importantly, the tumoricidal and TMZ sensitizing effects of BI2536 were observed across independent EGFRvIII glioblastoma clones that acquired resistance to EGFR inhibitors

Full access

presence of tumor-associated amplifications and mutations in the epidermal growth factor receptor (EGFR). Methods: CSF and matching tumor tissue were obtained from patients undergoing resection of HGGs. We determined wildtype EGFR (wtEGFR) DNA copy number amplification, as well as wtEGFR and EGFRvIII RNA expression, in tumor samples. We also characterized wtEGFR and EGFRvIII RNA expression in CSF-derived EVs. Results: EGFRvIII positive tumors had significantly greater wtEGFR DNA amplification (p=0·02) and RNA expression (p=0·002), and EGFRvIII positive CSF